ライフサイエンスコーパス: lactacystin

1 treatment with proteasome inhibitors (MG132, lactacystin).

2 ditions where the proteasome is inhibited by lactacystin.

3 teasome inhibition was tested with MG132 and lactacystin.

4 8644, 8Br-cAMP, and the proteasome inhibitor lactacystin.

5 locked by the selective proteasome inhibitor lactacystin.

6 es, including tunicamycin, geldanamycin, and lactacystin.

7 ed by chemical proteasome inhibitors such as lactacystin.

8 ntheses of omuralide, its C7-epimer, and (+)-lactacystin.

9 as E64, but not by the proteasome inhibitor lactacystin.

10 inhibited NOS2 induction and potentiation by lactacystin.

11 pha protein was partially blocked by ALLN or lactacystin.

12 in, was blocked by the proteasome inhibitor, lactacystin.

13 wild-type Gag or of the proteasome inhibitor lactacystin.

14 the ER induced by the proteasome inhibitor, lactacystin.

15 he same as the specific proteasome inhibitor lactacystin.

16 (NP(147-155)) was enhanced, particularly by lactacystin.

17 ited by the proteasome inhibitors, MG132 and lactacystin.

18 132, N-acetyl-leucyl-leucyl-norleucinal, and lactacystin.

19 a-1b peptide epitope even in the presence of lactacystin.

20 transfer protein inhibition were reversed by lactacystin.

21 cells with the proteasomal inhibitor ZLLL or lactacystin.

22 n is attenuated by the proteasome inhibitor, lactacystin.

23 y, mice were fed with CCl(4) with or without lactacystin.

24 ncanamycin) but not the proteasome inhibitor lactacystin.

25 ion of SMC CREB alone or in combination with lactacystin.

26 hibitor, 17-AAG and the proteasome inhibitor lactacystin.

27 ion with the proteasome inhibitors MG-132 or lactacystin.

28 cked by both BFA and the proteasomal blocker lactacystin.

29 rtially rescued with a proteasome inhibitor, lactacystin.

30 h nontoxic doses of the proteasome inhibitor lactacystin.

31 tors, including PDTC, CAPE, BAY 11-7085, and lactacystin.

32 hat is inhibited by the proteasome inhibitor lactacystin.

33 ells is blocked by the proteasomal inhibitor lactacystin.

34 anti-DR5 antibody or anti-DR5 antibody plus lactacystin.

35 of the highly specific proteasome inhibitor lactacystin.

36 was prevented by the proteasomal inhibitor, lactacystin.

37 ndosomal coat protein Hrs from inhibition by lactacystin.

38 Bilateral microinjections of lactacystin (1.25 microg/side) into the mouse medial for

39 lls pretreated with the proteasome inhibitor lactacystin (10 microM) for 2 h.

40 osine (40 microCi) for 20 min and chased +/- lactacystin (10 microM) for up to 4 h.

41 Lactacystin (10 microM), a selective proteasome inhibito

42 MG132 or lactacystin (10 microm), inhibitors of the proteasome pa

43 yl-leucyl-leucine vinyl sulfone (Z-L3VS) and lactacystin, 2) L chain degradation occurs early in the

44 The use of inhibitors, including lactacystin (a proteosome-specific inhibitor), suggests

45 Lactacystin, a potent inhibitor of the proteasome pathwa

46 wild-type and mutant G6Pase is inhibited by lactacystin, a potent proteasome inhibitor.

47 ncreased in cells that had been treated with lactacystin, a proteasome inhibitor, and thapsigargin, a

48 e endoplasmic reticulum-Golgi transport, and lactacystin, a proteasome inhibitor.

49 iated by ubiquitin-proteosome degradation as lactacystin, a proteosome inhibitor, reverses these effe

50 ere found to be protected by the presence of lactacystin, a protesome inhibitor.

51 Treatment with lactacystin, a selective inhibitor of the proteasome, ca

52 Treatment of HL-60 cells with lactacystin, a selective inhibitor of the proteasome, ex

53 egradation of TR was specifically blocked by lactacystin, a selective inhibitor of the ubiquitin-prot

54 IRS-1 can be prevented by pretreatment with lactacystin, a specific inhibitor for proteasome degrada

55 This decrease was reversed by lactacystin, a specific inhibitor of the 26 S proteasome

56 thylsulfonylfluoride, caspase inhibitors, or lactacystin, a specific inhibitor of the 26S proteasome.

57 Treatment with lactacystin, a specific inhibitor of the proteasome, sig

58 Lactacystin, a specific proteasome inhibitor, blocks the

59 Lactacystin, a specific proteasome inhibitor, did not ap

60 cause it was inhibited by preincubation with lactacystin, a very specific proteasome inhibitor.

61 In contrast, lactacystin added 48 h after iNOS induction led to the a

62 Lactacystin added prior to cytokine stimulation prevente

63 xamined, the proteasome inhibitors MG132 and lactacystin affected Stat4, Stat5 and Stat6 turnover by

64 Lactacystin also completely blocked the LPS-induced expr

65 Lactacystin also enhanced the recovery of one Kd-restric

66 Importantly, lactacystin also prevented LPS-induced shock in mice.

67 AF-cmk) and clasto-lactacystin beta-lactone (lactacystin), an inhibitor of both TPPII and the proteas

68 own-regulation of cyclin D1 was inhibited by lactacystin, an inhibitor of 26S proteosome, suggesting

69 protein synthesis inhibitor cycloheximide or lactacystin, an inhibitor of the 20S proteasome.

70 In contrast, lactacystin, an inhibitor of the proteasome, inhibits HM

71 We found that lactacystin, an irreversible proteasome inhibitor, cause

72 ome is a likely site for MafA degradation as lactacystin, an irreversible proteasome inhibitor, cause

73 The degradation was inhibitable by lactacystin, an irreversible proteasome inhibitor.

74 s assessed by treatment of infected APC with lactacystin and brefeldin A, suggesting that the Ags are

75 Lactacystin and calpain inhibitor I, specific inhibitors

76 growth was induced by proteasome inhibitors (lactacystin and clasto-lactacystin beta-lactone) and was

77 bitors, but not by the proteasomal inhibitor lactacystin and concluded that the proteasome was only i

78 The proteasome inhibitors, lactacystin and epoxomicin, attenuated MIP-1beta induced

79 ocked by the proteasome-specific inhibitors, lactacystin and epoxomicin.

80 AAF-cmk was more potent than lactacystin and irreversibly blocked Shigella-induced ap

81 ovastatin arrest) unexpectedly abrogates the lactacystin and lovastatin pro-drug inhibition of the pr

82 Proteasome inhibitors lactacystin and MG-132 prevented the PAF-induced depleti

83 1alpha was reversed by proteosome inhibitors lactacystin and MG-132.

84 Inhibitors of the 26 S proteasome, lactacystin and MG132, block the TCDD-induced turnover o

85 be blocked by inhibiting the proteasome with lactacystin and MG132.

86 s not inhibited by the proteasome inhibitors lactacystin and N-acetyl-L-leucyl-L-leucyl-L-norleucinal

87 thyl ketone and was relatively unaffected by lactacystin and N-tosyl lysyl chloromethyl ketone.

88 ath and mitochondrial dysfunction induced by lactacystin and other pharmacological inhibitors of the

89 e drug-enhanced degradation was decreased by lactacystin and other proteasome inhibitors.

90 f MG132 or the specific proteasome inhibitor lactacystin and promoted by opioid agonist.

91 In contrast to ALLN, lactacystin and PS341, two specific proteasome inhibitor

92 served both with chemical inhibitors such as lactacystin and pyrrolidinedithiocarbamate as well as wi

93 nder normal conditions and were increased by lactacystin and thapsigargin treatment, and growth of L1

94 inated protein and reduced cell viability in lactacystin and thapsigargin-treated cells.

95 bitor of the chymotrypsin-like activity than lactacystin and the peptide vinyl sulfone NLVS.

96 Both lactacystin and the specific proteasomal inhibitor epoxo

97 B activation (using the proteasome inhibitor lactacystin and using cells lacking either functional NF

98 asome inhibitors (proteasome inhibitor 1 and lactacystin) and in other cell types (NRK fibroblasts).

99 ree different proteasome inhibitors (MG-132, lactacystin, and bortezomib), and the mechanism underlyi

100 earance of the stub, even in the presence of lactacystin, and concomitantly inhibited remnant clearan

101 Ag expression was diminished by brefeldin A, lactacystin, and cycloheximide, but not by chloroquine,

102 The proteasome inhibitors MG132, lactacystin, and epoxomicin blocked PICT1 degradation, w

103 sensitivity to the inhibitors MG115, MG132, lactacystin, and epoxomicin.

104 tussis toxin, small interfering RNA for Rap, lactacystin, and expression of Rap1GAPII.

105 tment with the specific proteasome inhibitor lactacystin, and in combination with mannosidase inhibit

106 the proteasome inhibitors hemin, MG132, and lactacystin, and in the mouse ts85 cell line, which carr

107 Inhibitors of NF-kappaB signaling, lactacystin, and MG132 abolished the AR promoter respons

108 eatment with the proteosome inhibitors ALLN, lactacystin, and PSI [N-benzyloxycarbonyl-Ile-Glu-(O-t-b

109 BFA, lactacystin, and TAP inhibition blocked the recognition

110 rocess that requires ATP but is inhibited by lactacystin, and the lactacystin-sensitive turnover of u

111 in (pRb) phosphorylation that occurred after lactacystin application, and expression of a mutant pRb

112 inclusions formed at late time points after lactacystin application, the formation of ubiquitinated

113 dation of the CKIs, allowing lovastatin- and lactacystin-arrested cells to resume cell division.

114 evious studies in poly(Q) diseases have used lactacystin as an inhibitor--recent studies have shown t

115 ectively blocked by the proteasome inhibitor lactacystin as well as calpain I and II inhibitors; E2A

116 nduction of the unfolded protein response by lactacystin, as evidenced by the up-regulation of endopl

117 ct was prevented by the proteasome inhibitor lactacystin, as well as by rapamycin.

118 Pretreatment with the proteasome inhibitor lactacystin before the addition of GA resulted in the el

119 show that proteasome inhibition with clasto-lactacystin beta-lactone (4 microM, 1 h) stabilizes the

120 -Phe-chloromethylketone (AAF-cmk) and clasto-lactacystin beta-lactone (lactacystin), an inhibitor of

121 rentiation, the proteasome inhibitors clasto-lactacystin beta-lactone and carbobenzoxy-leucinyl-leuci

122 retase cleavage was not observed with clasto-lactacystin beta-lactone and thus, cannot be attributed

123 e BrAAP activity of the proteasome by clasto-lactacystin beta-lactone is also biphasic.

124 Treatment at 48 h with LLL but not clasto-lactacystin beta-lactone resulted in partial uncoupling

125 roteasome inhibitors (lactacystin and clasto-lactacystin beta-lactone) and was associated with elevat

126 oteasome inhibitors (NLVS, MG132, and clasto-lactacystin beta-lactone) were tested for their ability

127 he degradation of apoB was reduced by clasto-lactacystin beta-lactone, a potent proteasome inhibitor,

128 n was inhibited to a lesser extent by clasto-lactacystin beta-lactone, ALLN, and Nalpha-tosyl-L-pheny

129 en with another proteasome inhibitor, clasto-lactacystin beta-lactone, but not with an inhibitor of v

130 was controlled for using NH(4)Cl and clasto-lactacystin beta-lactone, respectively.

131 presence of the proteosome inhibitor clasto-lactacystin beta-lactone, suggesting that p12(DOC-1) may

132 y lactacystin, MG132, epoxomicin, and clasto-lactacystin beta-lactone.

133 roteasome inhibitors NLVS, MG132, and clasto-lactacystin beta-lactone.

134 However, proteasome-specific inhibitors, lactacystin-beta-lactone and epoxomicin, could not stabi

135 on of the 26S proteasome by MG115 and clasto-lactacystin-beta-lactone enhanced the accumulation of hi

136 as inactivated by the ester inhibitor clasto-lactacystin-beta-lactone severalfold faster than the wt,

137 Clasto-lactacystin-beta-lactone, the proteasome-specific inhibi

138 -L-leucyl-L-leucyl-L-norvalinal), and clasto-lactacystin-beta-lactone].

139 Cs), and the proteasome inhibitors MG132 and lactacystin block ER protein degradation in vitro.

140 In contrast, proteasome inhibitor MG-132 and lactacystin blocked both TNF-induced degradation of Ikap

141 y, in murine macrophage cell line RAW 264.7, lactacystin blocked iNOS degradation when added 48 h aft

142 The proteasome inhibitor lactacystin blocked the proteasome-mediated proteolysis

143 atment with proteasome inhibitors, MG-132 or lactacystin, blocked the degradation of the C/EBPalpha p

144 Proteasome inhibitors, MG132 and lactacystin, blocked the NO donor-induced reduction in I

145 f Rap1 and treatment with pertussis toxin or lactacystin blocks these effects.

146 N-acetyl-L-leucyl-L-leucyl-L-norleucinal and lactacystin but not lysosome inhibitor leupeptin inhibit

147 mmonly used proteasome inhibitors, MG132 and lactacystin but not N-acetyl-Leu-Leu-norleucinal, suppre

148 the selective proteasome inhibitor MG-132 or lactacystin but not the lysosomal inhibitor chloroquin.

149 cked in the presence of proteasome inhibitor lactacystin, but lactacystin did not confer protection a

150 ein is prevented by the proteasome inhibitor lactacystin, by inhibitors of mitogen-activated protein

151 ersed by the proteasome inhibitors MG132 and lactacystin, by p19(arf), and by small interfering RNA (

152 Proteasomal inhibitors, lactacystin, Cbz-leucine-leucine-leucinal, and N-acetyl-

153 o death induced by the proteasomal inhibitor lactacystin compared with neurons derived from wild-type

154 ro and, conversely, the proteasome inhibitor lactacystin completely blocked the LPS-induced proteasom

155 The proteasome inhibitors MG-132 and lactacystin completely protected HDAC1 from the action o

156 hibitors (proteasome inhibitor I, MG-132, or lactacystin) decreased the extent of U50,488H-induced do

157 about 4 hours, and the proteasome inhibitor lactacystin delayed its clearance more than 16 hours.

158 inhibited by a potent proteasome inhibitor, lactacystin, demonstrating that G6PT is a substrate for

159 Bortezomib and lactacystin did not cause cellular toxicity at the regim

160 nce of proteasome inhibitor lactacystin, but lactacystin did not confer protection against cell cycle

161 of the highly specific proteasome inhibitor lactacystin did not detectably affect ligand-induced pro

162 AAF-cmk and lactacystin did not impair macrophage phagocytosis or th

163 In addition, lactacystin dysregulated mitogen-activated protein kinas

164 We report here that the addition of MG132 or lactacystin, each a specific inhibitor of cellular prote

165 ch as acetyl-Leu-Leu-norleucinal, MG132, and lactacystin efficiently block LeTx cytotoxicity, whereas

166 etyl-L-leucinyl-L-leucinyl-L-norleucinyl and lactacystin enhance their stability.

167 ical purification of peptides confirmed that lactacystin enhanced the generation of Kd-NP(147-155) co

168 e at these sites was inhibitable by LLnL and lactacystin, epitope-containing species were still not p

169 however, the specific proteosome inhibitor, lactacystin, failed to do so.

170 in levels was also prevented by rapamycin or lactacystin, further indicating a proteasomal mediated d

171 inhibited (N -acetyl-Leu-Leu-norleucinal or lactacystin) G6PD activity increased.

172 Specific proteasome inhibitors such as lactacystin greatly stabilize p35 in vivo.

173 el of alpha(1)-ATZ expression, we found that lactacystin had a similar inhibitory effect on degradati

174 n of proteasomal protein degradation by beta-lactacystin has no effect of its own on extinction or on

175 r, while poly(Q) aggregation was enhanced by lactacystin in our inducible PC12 cell model, aggregatio

176 idase-independent manner and was arrested by lactacystin, in response to the posttranslational inhibi

177 Lactacystin increased IkappaB-beta expression in the abs

178 Lactacystin increased NOS2 promoter activation after 24

179 Surprisingly, both LLnL and lactacystin increased rather than inhibited the expressi

180 Lactacystin increased ubiquitinylated MTP and prevented

181 a in the presence of a proteasome inhibitor, lactacystin, indicating that cetuximab acts mainly at th

182 xy-L-leucyl-L-leucyl-L-leucinal (MG-132), or lactacystin induced NF-kappaB activation as indicated by

183 ive properties against proteasome inhibitor (lactacystin) -induced nigrostriatal degeneration.

184 roved behavioral performances and attenuated lactacystin-induced DA neuron loss, proteasomal inhibiti

185 2, Cdk4, or Cdk6 was also protective against lactacystin-induced death.

186 Furthermore, lactacystin-induced increase of cleaved PARP, cleaved ca

187 1 expression vector transfection rescued the lactacystin-induced injury.

188 Lactacystin-induced neurite outgrowth was blocked by the

189 ubiquitin-proteasome system and suggest that lactacystin induces apoptosis in part by disabling the u

190 that FVIII is degraded within the cell by a lactacystin-inhibitable pathway, implicating the cytosol

191 eu-norleucinal) and the proteosome inhibitor lactacystin inhibited the HRG-induced down-regulation of

192 We have found that the proteasome inhibitor, lactacystin, inhibited p130 downregulation in T98G cells

193 115, N-acetyl-leucyl-leucyl-norleucinal) and lactacystin, inhibited the degradation of short-lived pr

194 MG132 and lactacystin, inhibitors of the ubiquitin-proteasome path

195 s LPS-independent caveolin-1 expression, and lactacystin inhibits LPS-triggered caveolin-1 responses.

196 In lactacystin-injected eyes, the programmed degradation of

197 the Bcl-2 level, which was suppressed after lactacystin injection.

198 e proteasome was reduced by 60% to 70% after lactacystin injection.

199 PI3K inhibitors or the proteasome inhibitor lactacystin interfere with this process.

200 A proteasome inhibitor, lactacystin, interfered with bICP0-induced degradation o

201 In vivo, stereotactic microinjection with lactacystin into right median forebrain bundle (MFB) of

202 r basal conditions, the proteasome inhibitor lactacystin (LAC) increased apoB100 recovery, indicating

203 Lactacystin (lac) pretreatment of preconditioned hearts

204 wever, inhibition of proteasomal function by lactacystin largely prevented the degradation of ABCA1.

205 loxycarbonyl (Z)-Leu-Leu-leucinal (MG132) or lactacystin (LC) did not enhance the levels of SMA, but,

206 ia cells exposed to the proteasome inhibitor lactacystin (LC).

207 nNOS that inhibition of the proteasome with lactacystin leads to the accumulation of immunodetectabl

208 carbobenzoxy-leucyl-leucyl-phenylalaninal or lactacystin led to a loss of dually phosphorylated, acti

209 some inhibitors N-Ac-Leu-Leu-norleucinal and lactacystin led to accumulation of PKC eta proteolytic p

210 6S proteasome with two inhibitors, ALLnL and lactacystin, led to an elevation of the N-myc protein st

211 ith either chloroquine or leupeptin, but not lactacystin, led to intracellular stabilization, implica

212 In the presence of the proteasome inhibitor, lactacystin, light results in the formation of a high mo

213 VELCADE trade mark bortezomib or injection), lactacystin, LLnL) and cyclin-dependent kinase inhibitor

214 The proteasome inhibitor, lactacystin, markedly increased MMP-2 levels and invasio

215 an inhibitor--recent studies have shown that lactacystin may also affect lysosomal function.

216 in the presence of the proteasome inhibitor lactacystin, Met fails to redistribute from the plasma m

217 teolysis were blocked by specific inhibitors lactacystin, MG-132, and ZLLF-CHO.

218 Treatment with the proteasomal inhibitors lactacystin, MG132, and N-acetyl-l-leucinyl-l-leucinyl-l

219 NF-kappaB pathway by IkappaB superrepressor, lactacystin, MG132, arsenic trioxide, and phenylarsine o

220 degradation of alpha(1)-ATZ was inhibited by lactacystin, MG132, epoxomicin, and clasto-lactacystin b

221 intraperitoneally 7 days before or after the lactacystin microinjection until the mice were sacrifice

222 d by selective inhibitors of the proteasome (lactacystin, NLVS, and epoxomycin) and by an antisense o

223 The effect of lactacystin on mitochondrial degradation was assessed by

224 oteasome inhibitors Cbz-Leu-Leu-Leucinal and lactacystin on the ability of mouse fibroblast cells to

225 Furthermore, the effects of LLnL and lactacystin on the expression of different categories of

226 last cultures with the proteasome inhibitors lactacystin or bortezomib (Velcade).

227 Treatment with the proteasome inhibitors lactacystin or epoxomicin reversed m155 down-regulation

228 on pathways, since it is prevented by either lactacystin or epoxomicin, two inhibitors of proteasomal

229 ment with the proteasome inhibitors MG132 or lactacystin or high concentrations of leupeptin, indicat

230 t, treatment with the proteasome inhibitors (lactacystin or MG-132) caused an accumulation of Nrf2 as

231 ion of 26S proteasome activity by the use of lactacystin or MG132 completely blocked IGF-mediated deg

232 s was inhibited by the proteasome inhibitors lactacystin or MG132.

233 Gag p55 immune complexes in the presence of lactacystin or of bafilomycin indicated that the mechani

234 istration of either the proteasome inhibitor lactacystin or the lysosome inhibitor chloroquine, indic

235 Inhibition of the proteasome by lactacystin or Velcade increases the levels of R555W mis

236 inhibitors (30 micromol/L ALLN, 2 micromol/L lactacystin, or 100 nmol/L MG132) reduced the BMK1-media

237 with proteasomal inhibitors (MG-132, MG-115, lactacystin, or proteasome inhibitor I), but not lysosom

238 scle proteolysis, while proteasome inhibitor lactacystin partially blocks it.

239 ion of Akt and ERK1/2, which was reversed by lactacystin pretreatment.

240 atment of SMCs with the proteasome inhibitor lactacystin prevented decreases in CREB content.

241 the proteasomal pathway with either MG132 or lactacystin prevented rapamycin from partially reversing

242 cells with proteasome inhibitors MG-132 and lactacystin prevented the decrease in the phosphoserine-

243 Both AAF-cmk and lactacystin prevented the maturation of pro-caspase-1 an

244 ilomycin-A1), but not proteasome inhibition (lactacystin), prevented the reduction in CFTR levels.

245 e specific inhibitor of proteasome function, lactacystin, prevented intracellular degradation of Z al

246 two proteins with the proteasome inhibitor, lactacystin, prevented lipopolysaccharide + cycloheximid

247 aldehydes, and the mechanistically different lactacystin, prevented NSAID gastropathy.

248 Treatment of cells with lactacystin prevents PAT1 degradation and retains its nu

249 found that proteasomal inhibitors, MG132 and lactacystin, prolong the cellular half-life of LRP.

250 FL-expressing cells, mimicking the effect of lactacystin proteasomal inhibition, indicating that CAIR

251 was demonstrated by the ability of MG-132 or lactacystin (proteasome inhibitors) to block the enhance

252 TR1 was blocked by the proteasome inhibitors lactacystin, proteasome inhibitor 1, and MG132.

253 Similarly, lactacystin protected against endothelial apoptosis indu

254 Proteasome inhibitors MG132 and lactacystin protected the cells against IFN-gamma-induce

255 Although the specific proteasome inhibitor lactacystin provides marginal protection against GA-indu

256 Lactacystin reduced initial degradation of IkappaB-alpha

257 Lactacystin reduced the initial accumulation of NOS2 mRN

258 Inhibition of proteasomal degradation with lactacystin restored L18A/L25A protein expression, altho

259 ent with the proteasome inhibitors MG132 and lactacystin resulted in the stabilization of YY1 protein

260 ells with the specific proteasome inhibitor, lactacystin, resulted in a 3-fold increase in alpha4 in

261 Use of a proteasome inhibitor, lactacystin, resulted in increased expression of GCase,

262 ells to the proteasome inhibitors, MG132 and lactacystin, resulted in inhibition of proteasomal activ

263 acetyl-leucyl-leucyl-norleucinal (ALLN), and lactacystin, salinosporamide A was found to be the most

264 volved HER2 degradation, which was partially lactacystin sensitive and thus proteasome dependent.

265 Purified ER fractions contain lactacystin-sensitive and E64-insensitive proteasome act

266 Rapid lactacystin-sensitive degradation could be conferred on

267 Based on the mannosidase- and lactacystin-sensitive properties of intracellular turnov

268 ATP but is inhibited by lactacystin, and the lactacystin-sensitive turnover of ubiquitinated proteins

269 that was subject to rapid degradation by the lactacystin-sensitive ubiquitin/proteasome system and an

270 (N-acetyl-leucinyl-leucinyl-norleucinal and lactacystin) significantly increased the cell levels of

271 Lactacystin slowed the degradation of the mutant protein

272 MG132 or lactacystin, specific inhibitors of 26S proteasome, bloc

273 cells with the specific proteasome inhibitor lactacystin, suggesting a normal regulation of the p53-M

274 Met-AL, MDMX degradation is not inhibited by lactacystin, suggesting that degradation occurs by a pro

275 inal plus N-acetyl-Leu-Leu-methioninal or by lactacystin, suggesting the involvement of proteasomes.

276 nts with the proteasome inhibitors MG132 and lactacystin that did not affect NO production.

277 Concentrations of lactacystin that inactivated more than 90% of the ChT-L

278 -Nle-CHO (ALLN), the calpain I inhibitor, or lactacystin, the 20 S proteasome inhibitor, blocked the

279 By using the specific proteasome inhibitor lactacystin to examine IkappaB degradation, we observed

280 Addition of the 26S proteasome inhibitor lactacystin to influenza C virus-infected or seg 6 ORF c

281 nal (LLnL) and the highly specific inhibitor lactacystin, to examine the role of proteasomes in gener

282 ([(3)H]tyrosine-labeled) was similar between lactacystin-treated and control islets despite a 51% dec

283 itatively similar to p53-Ub((n)) detected in lactacystin-treated cells.

284 (pro)insulin in the extracellular medium of lactacystin-treated islets (0.52 +/- 0.16 cpm/microunits

285 tal immunoreactive (pro)insulin secretion by lactacystin-treated islets.

286 ynuclein did not influence the percentage of lactacystin-treated neurons harboring cytoplasmic ubiqui

287 Lactacystin treatment decreased the p32 zymogen and evok

288 Lactacystin treatment disrupted the HLA-A2 clusters, but

289 Lactacystin treatment of HL-60 cells induced proteolytic

290 Lactacystin treatment of the donor male MHC-I-deficient

291 Our results showed that, following lactacystin treatment, levels of endogenous KLF4 increas

292 Neither LLnL nor lactacystin was able to completely block the expression

293 OS2 expression at low concentrations or when lactacystin was added subsequent to cytokines.

294 ubiquitin-proteasome pathway (UPP) in vivo, lactacystin was injected into the vitreous humor of the

295 endoplasmic reticulum (ER)) and restored by lactacystin (which inhibits proteasomal degradation).

296 ity was blocked by intravitreal injection of lactacystin, which also was found to increase AA-NAT act

297 nhibitors of proteasome function and also by lactacystin, which blocks proteasome activity by covalen

298 full-length Gag polyprotein was sensitive to lactacystin, which depletes the levels of free ubiquitin

299 y was obtained with the proteasome inhibitor lactacystin, which in short-term 2-h experiments enhance

300 P-dependent epitopes was blocked by LLnL and lactacystin, while a TAP-independent epitope that is pro